Heart patients might have been puzzled to be given a prescription for an antibiotic as part of their preventative treatment. After all, how's that supposed to stop a heart attack?
Antibiotic therapy is based on the theory that the respiratory virus Chlamydia pneumoniae plays a part in atherosclerosis, or furring of the arteries. The antibiotic kills the virus, and the furring stops.
Fine, in theory. In fact, antibiotic treatment does nothing to stop atheroslerosis, as two major studies have just discovered. The first involved 4,012 patients with stable coronary artery disease who were either given the antibiotic azithromycin or a placebo, and the second recruited 4,162 patients with acute coronary syndrome who were given either the antibiotic gatifloxacin or placebo. In neither trial did the antibiotic group fare any better than those given a placebo.
So is this the end of the road for the C pneumoniae theory? It may be premature to throw it in the overcrowded rubbish bin of discarded medical theories, although the new studies put a big question-mark over it. The virus has been detected in around 40 per cent of atherosclerotic plaques, and mice and rabbits inoculated with the virus have developed inflammatory lesions in arteries.
This could be put another way. The majority of heart patients don't have the virus, and animal trials are never a safe indication of similar activity in humans (apart from being needlessly cruel and pointless). And the fact that the virus is present in a minority of plaques doesn't prove a causal link between the two.
It could also be because antibiotic therapy is a case of being too little, too late. Artery disease can begin as early as the age of 15, and so every schoolchild would need to be screened for antibiotic therapy to be effective.
As it is, it's just another useless drug in the fight against heart disease. Lifestyle changes, anyone?
(Source: New England Journal of Medicine, 2005; 352: 1637-45, and 1646-54).
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